Uric acid is a final product of a purine metabolism in humans. The purine nucleotide is generated by degradation of a nucleic acid in the cell, ATP that is an energy source in a living body, and the like, or is absorbed from a meal. The purine nucleotide is metabolized to uric acid via hypoxanthine and xanthine. Uric acid is a final product of the purine metabolism in the higher primates including human as urate oxidase (uricase) is genetically silenced in these species. In many other mammals, uric acid is oxidized by uricase, and metabolized to allantoin.
About 98% of uric acid is present in the form of sodium urate in a body liquid (Non Patent Literature 1).
Since the solubility of sodium urate at physiological pH conditions is 6.4 mg/dL (Non Patent Literature 1), 7 mg/dL or more of the blood uric acid level beyond the solubility in the body liquid is defined as hyperuricemia (Non Patent Literature 2).
If the hyperuricemia persists, urate is crystallized and precipitated in the body liquid, which cause gout arthritis, gouty kidney, gouty node, urolithiasis, a renal function disorder and the like (Non Patent Literature 3).
In addition, in recent years, the hyperuricemia is known to be complicated with lifestyle diseases such as hypertension, hyperlipidaemia, impaired glucose tolerance and obesity in high rate (Non Patent Literatures 4, 5, 6 and 7), and such complications are known to increase the incidence rate of cardiovascular or cerebrovascular disorders.
The hyperuricemia is reported to be present in 20% or more of adult males in Japan, and tends to increase even now due to westernized lifestyle and the like (Non Patent Literature 8). As for the classification of hyperuricemia, the overproduction of uric acid is reported to be 12%, the decreased uric acid excretion to be 60% and the combined type to be 25% (Non Patent Literature 9). Thus, the decreased uric acid excretion is seen in 85% that is the sum of 60% of the decreased uric acid excretion and 25% of the combined type, which suggests the importance of the decreased uric acid excretion with respect to the cause of hyperuricemia.
Uric acid is mainly excreted from a kidney. In humans, about 70% is excreted from the kidney, and 30% is excreted from extra-renal pathway such as a bile or a saliva, a sweat and the like. The uric acid is filtered by 100% in a renal glomerulus, and then most part of it is re-absorbed in a proximal tubule, and about 10% is excreted in a terminal urine (Non Patent Literatures 3 and 10). Thus, it is suggested that uric acid excretion is strictly regulated by the re-absorption.
Since uric acid is present as an organic acid at physiological pH conditions, it was expected that a transporter responsible for re-absorption of uric acid has similar structural characteristics with an organic anion transporter family proteins. In recent years, URAT1 was identified as a transporter responsible for re-absorption of uric acid, which is present in the proximal tubule (Non Patent Literature 11). URAT1 is a 12-transmembrane transporter belonging to the SLC family. Northern blotting analysis showed that an expression of a URAT1 gene is localized in the kidney of an adult and fetus. It became clear from immunohistochemical analysis using anti-human URAT1 antibody that an URAT1 protein is present on a luminal surface of the proximal tubule. Furthermore, since uric acid is incorporated when URAT1 is expressed in a xenopus oocyte, it was confirmed that URAT1 can transport of uric acid (Non Patent Literature 11).
Further, it became clear that loss of function caused by mutations of the URAT1 gene leads to renal hypouricemia, and thus importance of URAT1 with respect to uric acid excretion came to the fore (Non Patent Literatures 11 and 12).
Currently used uricosuric agents, benzbromarone and probenecid have been shown to inhibit uric acid-transport activity of URAT1, and importance in the uric acid excretion of URAT1 has been cleared pharmacologically as well (Non Patent Literature 13).
From these, it is regarded that a drug inhibiting URAT1 can reduce the blood uric acid level by suppressing re-absorption of uric acid in the proximal tubule and by accelerating the uric acid excretion, and the drug inhibiting URAT1 is useful as an agent for treating or preventing pathological conditions associated with uric acid, specifically, hyperuricemia, gouty node, gout arthritis, gouty kidney, urolithiasis and renal function disorders. In addition, the drug inhibiting URAT1 is also useful as an agent for treating or preventing hypertension, hyperlipidaemia, abnormal glucose tolerance, obesity, a coronary artery diseases and cerebrovascular disorders, which are associated with hyperuricemia.
Incidentally, as a compound that has URAT1 inhibitory action, for example, Patent Literature 1 discloses a compound of the general formula described below.

Patent Literature 2 discloses a compound of the general formula described below.

Patent Literature 3 discloses a compound of the general formula described below.

Patent Literature 4 discloses a compound of the general formula described below as a PDE5 (phosphodiesterase 5) inhibitor.

Patent Literature 5 discloses a compound of the general formula described below as a PDE5 inhibitor.R1—SO2NHCO-A-R2 
Patent Literature 6 discloses a compound of the general formula described below as a 17β HSD (17β-hydroxysteroid dehydrogenase) type 5 inhibitor.
